The Expression Regulation and Biological Function of Autotaxin.
The Expression Regulation and Biological Function of Autotaxin.
复制标题
DOI：
10.3390/cells10040939
复制
发表时间：
2021-04-19
期刊：
影响因子：
6
通讯作者：
Zhang J
中科院分区：
文献类型：
--
作者：
Zhang X;Li M;Yin N;Zhang J
自分泌运动因子（ATX）是一种分泌型糖蛋白，是产生细胞外溶血磷脂酸（LPA）的关键酶。LPA与细胞膜上的至少六种G蛋白偶联受体LPAR 1 -6相互作用，以通过不同的G蛋白（如Gi/0、G12/13、Gq/11和Gs）激活各种信号转导途径。ATX-LPA轴在生理和病理过程中起重要作用，包括胚胎发生、肥胖和炎症。ATX是转移性癌症中前40个最不受调控的基因之一，ATX-LPA轴参与不同类型癌症的发展，如结直肠癌、卵巢癌、乳腺癌和胶质母细胞瘤。ATX表达在转录、转录后和分泌水平上受到多方面的控制。肿瘤微环境中的ATX和LPA不仅促进细胞增殖、迁移和存活，还增加炎症相关回路的表达，这导致癌症患者的预后不良。目前，ATX被认为是潜在的癌症治疗靶点，并且已经开发了越来越多的ATX抑制剂。本文就ATX的表达调控机制及其在肿瘤发生发展中的作用作一综述。
Autotaxin (ATX) is a secreted glycoprotein and functions as a key enzyme to produce extracellular lysophosphatidic acid (LPA). LPA interacts with at least six G protein-coupled receptors, LPAR1-6, on the cell membrane to activate various signal transduction pathways through distinct G proteins, such as Gi/0, G12/13, Gq/11, and Gs. The ATX-LPA axis plays an important role in physiological and pathological processes, including embryogenesis, obesity, and inflammation. ATX is one of the top 40 most unregulated genes in metastatic cancer, and the ATX-LPA axis is involved in the development of different types of cancers, such as colorectal cancer, ovarian cancer, breast cancer, and glioblastoma. ATX expression is under multifaceted controls at the transcription, post-transcription, and secretion levels. ATX and LPA in the tumor microenvironment not only promote cell proliferation, migration, and survival, but also increase the expression of inflammation-related circuits, which results in poor outcomes for patients with cancer. Currently, ATX is regarded as a potential cancer therapeutic target, and an increasing number of ATX inhibitors have been developed. In this review, we focus on the mechanism of ATX expression regulation and the functions of ATX in cancer development.
登录
查看更多内容
影响因子：
3.7
作者：
David M;Wannecq E;Descotes F;Jansen S;Deux B;Ribeiro J;Serre CM;Grès S;Bendriss-Vermare N;Bollen M;Saez S;Aoki J;Saulnier-Blache JS;Clézardin P;Peyruchaud O
通讯作者：
Peyruchaud O
影响因子：
4.8
作者：
Benesch, Matthew G. K.;Tang, Xiaoyun;Brindley, David N.
通讯作者：
Brindley, David N.
影响因子：
4.8
作者：
D'Souza, Kenneth;Kane, Daniel A.;Kienesberger, Petra C.
通讯作者：
Kienesberger, Petra C.
影响因子：
5.3
作者：
Chen C;Ochoa LN;Kagan A;Chai H;Liang Z;Lin PH;Yao Q
通讯作者：
Yao Q
影响因子：
3.9
作者：
Benesch, Matthew G. K.;Ko, Yi M.;McMullen, Todd P. W.
通讯作者：
McMullen, Todd P. W.